Conventionally, implantable cardiac devices (ICDs), including “pacemakers,” have emphasized stimulating the heart. The heart is situated in a single location in the body so it is relatively easy to place an ICD in close proximity to cardiac muscle tissue. The human vascular system, on the other hand, includes vast networks of blood vessels that are spread pervasively throughout the body, so it is relatively difficult to gain ICD control of vascular muscle tissue in the linings of arteries and veins.
Conventional ICDs have avoided or ignored controlling the vascular muscle layers of arteries and veins for additional reasons. Cardiac muscle tissue differs from both skeletal muscle tissue and smooth muscle tissue by being quickly responsive to electrical stimulation, whereas the smooth muscle tissue surrounding arteries and veins is relatively slow to react. Conventional circulatory control was easily achieved by stimulating the responsive and easily accessible cardiac muscle tissue, with its largely self-contained electrical system. The smooth muscle tissue of the vascular system, by comparison, was more difficult to access and control.
The smooth muscle layers of arteries are controlled by the sympathetic and parasympathetic nervous subsystems with control often originating in the brain, yet not under direct conscious control. A host of hormones and pharmaceuticals that bind to receptors on smooth muscles and exert their own influences can interfere with artificial electrical control of these smooth muscle layers.
When the body controls its own vascular system, the aforementioned layer of smooth muscle between elastic lamina (layers) of an artery typically opens and closes the bore or “lumen” of the artery. Closing an arterial lumen is referred to as vasoconstriction, which typically increases blood pressure because the circulatory system has a relatively inflexible volume capacity. Opening an arterial lumen is referred to as vasodilation and typically lowers the blood pressure.
Control over the same parameters that are ubiquitously present in many artificial hydraulic systems can lead to more masterful treatment of human circulatory diseases as well. To treat hypertension (high blood pressure) or hypotension (low blood pressure) for example, treatments include control over the heart as pump, over the volume capacity of the system (for example, using diuretics), and/or over the volume of fluid in the system. By nature, a human body in good health controls these three factors simultaneously. For example, when increased blood perfusion is needed for physical exertion, the body may deliver more blood to the exercising tissues by simultaneously increasing the strength and speed of the pumping action and raising the blood pressure, by vasoconstriction.
The sympathetic and parasympathetic subsystems, which initiate vasoconstriction and vasodilation respectively, are not limited to controlling mere low-level operational aspects of the body corresponding to valves and sensors in a hydraulic machine. Rather, these nervous subsystems also play more profound roles in directing activities of daily living and emotions. During rest times, for example, vasodilation maintained by the parasympathetic subsystem may direct more blood to activities like digestion, with resultant feelings of relaxation, while during physical activity and stress, vasoconstriction initiated by the sympathetic subsystem may direct blood away from the digestive tract to skeletal muscles, with resultant feelings of strength and excitement.
Comprehensive control of the circulatory system, such as that accomplished by the body itself, can provide improved treatment for many circulatory maladies. For example, orthostatic hypotension (OSH) is a common geriatric disorder as well as a common side effect of many medications. It is generally described as a decrease of 10-20 millimeters of mercury (mmHg) or more in systolic blood pressure when posture changes from supine to standing—a horizontal to vertical change in posture. OSH can have neurogenic etiologies (e.g., diminished baroreceptor reflex); vestibular disorders; peripheral/central nervous system deficiencies; etc.) or non-neurogenic etiologies (e.g., cardiac pump failure, reduced blood volume, venous pooling, etc.). Device therapies that only elevate heart rate during an OSH episode (i.e., that target the non-neurogenic deficiencies) may fail if there is a lack of vasoconstriction due to reduced baroreceptor reflex. Similarly, treatments that only stimulate vasomotor sympathetic nerves (i.e., target only neurogenic deficiencies) may fail if there is a pronounced pumping failure. Thus, an implantable medical device therapy that can simultaneously compensate for both neurogenic and non-neurogenic influences on the circulatory system can be very advantageous in treating OSH and other disorders.
There is a need for an implantable device that takes advantage of the autonomic nervous system, resulting in simultaneous control of more types of muscle tissues in the circulatory system than just cardiac muscle tissue. Such an implantable device would control the cardio and vascular components of the cardiovascular system in a more organic and comprehensive manner than just controlling heart rate and other cardiac parameters via a conventional ICD.